Metabolic syndrome (MS) is closely linked to obesity and insulin resistance. Several epidemiological studies have attempted to find the robust link between MS and asthma control in children and it is still under debate. The crosstalk of adipokine imbalance and hyper-insulinemia with airway inflammation including hyperresponsiveness has been proposed as the probable mechanism along with other factors [1].

In this issue of the journal, Kumar et al. reported that in children with asthma between 10 to 15 y, the prevalence of insulin resistance (IR) and MS was 42.3% and 1.2% respectively [2]. The asthma control was significantly poorer among those with elevated serum insulin, triglycerides, and the presence of IR. It was a well-conducted study with the inclusion of the age group 10–15 y, thus assessing the pubertal hormonal effects on metabolic syndrome as well. In the current study, spirometry failed to reciprocate the relation with any of the parameters. The relationship of lung function in childhood asthma with IR, BMI, and MS studied extensively by Forno et al. revealed that patients with high BMI and IR had significantly low FEV1, FVC, and FEV1/FVC [3].

The authors have well incorporated all the metabolic parameters in their studies. However, increased serum leptin (pro-inflammatory) and decreased adiponectin (anti-inflammatory) constitute the biochemical shreds of evidence for the relation between childhood obesity and asthma. In a study on Southeast Europe children, there were significantly higher levels of leptin in the overweight with asthma group in comparison with the asthma group. Similarly, HOMA-adiponectin levels were higher in the overweight with asthma group than in the asthma group [4]. Hence, a cohort study assessing the correlation between serum leptin, adiponectin, asthma control, and lung functions may add further biochemical evidence.

An obesity-asthma is a chicken-egg question, and this is regarded to be a distinctive phenotype from asthma in children, with more of the Th-1 type, poor asthma control, poor lung function, and poor response to inhaled corticosteroids. The relationship between BMI with asthma, atopy, IgE levels, and gender predominance is quite interesting. In the National Health and Nutrition Examination Survey (NHANES) III, of 4 to 17 y, the prevalence of asthma and atopy increased significantly with increasing BMI [5].

In conclusion, the present study provokes awareness about metabolic dysregulation in the context of pediatric asthma in a cross-sectional view. However, a well-conducted cohort study involving a target control of metabolic syndrome and its correlation with asthma control and lung functions might be more appropriate to answer the million-dollar question of causation or association.